Tabaquismo factor de riesgo cardiovascular y disfuncion endotelial Ricardo Mora MD
Tabaquismo como factor de riesgo endotelial y disfuncion endotelial; Dr. Ricardo Mora Moreno R2C; IMSS UMAE T1; León, Guanajuato, Mexico; 09 de Noviembre del 2017
Lipid, liver related and other clinical parameters affect study of cigarette ...IJARIIT
Background and objective: Cigarette smoking is one of the 10 greatest contributors to global death and disease.
Cigarette smoke consists of many chemicals, including cytotoxic, carcinogenic and free radicals, therefore it affects many
organs if not all. This work is directed to evaluate the effects of dose response patterns of tobacco exposure on liver tissue,
through assessing some serum biochemical parameters related to liver efficiency.
Methods: This study was done in Kirkuk province. It was conducted on (75) healthy male subjects, their ages ranged from
20 to 40 years. They were divided into three groups; 25 heavy smokers, 25 moderate smokers, and 25 non-smokers. Blood
was withdrawn for estimation of serum liver function test, lipid profile, and protein electrophoresis.
Results: There were statistically significant elevations in serum alkaline phosphatase (ALP), alanine transaminase (SGPT)
and aspartate aminotransferase (SGOT) activities in heavy smokers while serum total bilirubin significantly was lower
compared to nonsmokers. Serum total protein and albumin were significantly lower in heavy smokers comparing to nonsmokers.
The results of serum protein arose gel-electrophoresis showed significant changes in serum protein fractions in
smoker groups. The mean level of serum total cholesterol, triglyceride, LDL, and VLDL was significantly higher in heavy
smoker group, while serum HDL level had a significantly lower value.
Relative risk of cardiovascular morbidity is increased in Chronic Kidney Disease (CKD). According to current KDIGO guideline
cardiovascular risk can be estimated from Glomerular Filtration Rate (GFR) and proteinuria.
Tabaquismo factor de riesgo cardiovascular y disfuncion endotelial Ricardo Mora MD
Tabaquismo como factor de riesgo endotelial y disfuncion endotelial; Dr. Ricardo Mora Moreno R2C; IMSS UMAE T1; León, Guanajuato, Mexico; 09 de Noviembre del 2017
Lipid, liver related and other clinical parameters affect study of cigarette ...IJARIIT
Background and objective: Cigarette smoking is one of the 10 greatest contributors to global death and disease.
Cigarette smoke consists of many chemicals, including cytotoxic, carcinogenic and free radicals, therefore it affects many
organs if not all. This work is directed to evaluate the effects of dose response patterns of tobacco exposure on liver tissue,
through assessing some serum biochemical parameters related to liver efficiency.
Methods: This study was done in Kirkuk province. It was conducted on (75) healthy male subjects, their ages ranged from
20 to 40 years. They were divided into three groups; 25 heavy smokers, 25 moderate smokers, and 25 non-smokers. Blood
was withdrawn for estimation of serum liver function test, lipid profile, and protein electrophoresis.
Results: There were statistically significant elevations in serum alkaline phosphatase (ALP), alanine transaminase (SGPT)
and aspartate aminotransferase (SGOT) activities in heavy smokers while serum total bilirubin significantly was lower
compared to nonsmokers. Serum total protein and albumin were significantly lower in heavy smokers comparing to nonsmokers.
The results of serum protein arose gel-electrophoresis showed significant changes in serum protein fractions in
smoker groups. The mean level of serum total cholesterol, triglyceride, LDL, and VLDL was significantly higher in heavy
smoker group, while serum HDL level had a significantly lower value.
Relative risk of cardiovascular morbidity is increased in Chronic Kidney Disease (CKD). According to current KDIGO guideline
cardiovascular risk can be estimated from Glomerular Filtration Rate (GFR) and proteinuria.
HDL-cholesterol concentrations are inversely associated with CVD.When we consider cardiovascular mortality in women in terms of HDL.Causes of low HDL cholesterol.Lipoprotein subfractions suffer a shift after menopause towards a more atherogenic lipid profile.associations of HDL-C and HDL-P with cIMT and CHD.MESA (Multi-Ethnic Study of therosclerosis. Functional Versus Dysfunctional HDL. High concentrations of HDL - cholesterol are associated with high all-cause mortality in men and women.Improvement of HDL function without necessarily raising HDL-C
Evaluation of Biomarkers of Exposure and Cardiovascular & Pulmonary Function Endpoints in Adult Smokers Following Partial or Complete Substitution of Cigarettes with Electronic Cigarettes
ABSTRACT- Background: Microalbuminuria in hypertension has been described as an early sign of kidney damage
and a predictor for end stage renal disease and cardiovascular disease. More specifically it is seen amongst patients
suffering from hypertension.
Methods: This study was conducted at Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, India in the
department of emergency medicine and 84 subjects were included in the evaluation in the age of more than 30 years.
All patients were diagnosed by clinical examination, anthropometric measurement, blood pressure, urinary
microalbumin, and urinary creatinine. Statistical analysis was done by using SPSS, version 16.0 p-values were
calculated by chi-square test, ANOVA unpaired t-test. The p <0.05 was considered statistically significant.
Results: It was found that microalbuminuria among hypertensive patients increased steadily with the advancing age and
the duration of hypertension. The features of high urinary microalbumin 52.09±8.62 mg/24hr and the urinary creatinine
2.37±0.86mg/dl were prevalent in hypertensive patients and it increased in both male and female patients.
Conclusions: The prevalence of microalbuminuria in hypertensive individuals is high, and it revealed strong
association between microalbuminuria and hypertension. Our findings suggest that microalbuminuria could be a useful
marker to assess risk stratification and management of cardiovascular disease and renal disease.
Key words: Hypertension, Cardiovascular disease, Renal disease, Risk factors, Age factors, Urinary creatinine,
Urinary microalbumin
ASH13 Scott Hall and Robb Wolf — Evaluation of the Impact of a Paleolithic Di...Ancestral Health Society
Traditional cardiovascular risk factors including cholesterol may not provide the best tools for predicting individuals at risk for future cardiovascular disease and current insulin resistance. Novel and emerging evaluations of lipoproteins may provide a more accurate assessment of future cardiovascular risk. In an observational study of a small group of law enforcement officers, we studied the changes in both traditional and nontraditional risk factors when instructed in a “paleo” diet over 6 months. Overall, we found an encouraging impact on both traditional and nontraditional risk factors over the course of the study. It is proposed that a “paleo” diet supplemented with exercise has a positive effect on cardiovascular risk factors and may be a treatment recommendation for individuals at risk.
Blood biomarkers of smoking induced oxidative dna damage and oxidant-antioxidantUsama Mohamed El-Barrany
Abstract
Background: Smoking enhances oxidative stress by causing an imbalance between oxidants and antioxidants in the body leading to deleterious effects on various tissues. 8-hydroxy-2'-deoxyguanosine (8-OHdG) is a predominant form and a biomarker of free radical-induced oxidative lesions. This study aimed to estimate blood 8-OHdG level as a biomarker of oxidative DNA damage in active, passive as well as non-smokers and to assess its relation with lifestyle determinants as well as its effects on oxidant/antioxidant status.
Results: There were highly statistically significant higher levels of 8-OHdG, cotinine and malondialdehyde (MDA) and lower levels of superoxide dismutase (SOD) and total antioxidant capacity (TAC) in active smokers compared to both passive and non-smokers with no similar findings between the latter groups. There were no significant associations between 8-OHdG level and smoking habits, age, exercise, tea and coffee consumption as well as body mass index (BMI) among the 3 studied groups.
Conclusion: Smoking may induce oxidative stress not only through increasing the production of oxygen free radicals but also through weakening of the antioxidant defense mechanisms. Further studies are required to reach a concurrence on the background of 8-OHdG level.
Keywords: Smoking, Oxidative, Stress, Antioxidant, 8-OHdG.
Emotions are a form of non verbal communication that we use to reflect our physiological and mental state. We express emotions when we are dealing with everything around us even with our computers. Since we are becoming more dependent on computers in our lives, we need to design more interactive systems. In other words, we need to adapt computers to our needs as well as to our behavior; make computers emotionally intelligent, in order to be able to detect ours mood and make decisions based on that.
Lowering barriers to publishing biological data on the webBrad Chapman
Short 10 minute talk encouraging bioinformatics programmers to organize and reuse code targeted at making data easily available on the web. Current open source technologies are combined into a higher level framework. An example implementation using Google App Engine and existing bioinformatics libraries is presented.
A 60-minute webinar presented by Core Compliance & Legal Services and sponsored by LiveOffice.
Once You Archive Email, What's Next?
When it comes to email compliance, preparedness is key.
View this crash course in email compliance, and find out what else you need to know to protect yourself and your business.
You'll learn:
- What you are required to do after you capture electronic data
- What SEC and FINRA rules apply to email
- What types of communications require email supervision and more
HDL-cholesterol concentrations are inversely associated with CVD.When we consider cardiovascular mortality in women in terms of HDL.Causes of low HDL cholesterol.Lipoprotein subfractions suffer a shift after menopause towards a more atherogenic lipid profile.associations of HDL-C and HDL-P with cIMT and CHD.MESA (Multi-Ethnic Study of therosclerosis. Functional Versus Dysfunctional HDL. High concentrations of HDL - cholesterol are associated with high all-cause mortality in men and women.Improvement of HDL function without necessarily raising HDL-C
Evaluation of Biomarkers of Exposure and Cardiovascular & Pulmonary Function Endpoints in Adult Smokers Following Partial or Complete Substitution of Cigarettes with Electronic Cigarettes
ABSTRACT- Background: Microalbuminuria in hypertension has been described as an early sign of kidney damage
and a predictor for end stage renal disease and cardiovascular disease. More specifically it is seen amongst patients
suffering from hypertension.
Methods: This study was conducted at Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, India in the
department of emergency medicine and 84 subjects were included in the evaluation in the age of more than 30 years.
All patients were diagnosed by clinical examination, anthropometric measurement, blood pressure, urinary
microalbumin, and urinary creatinine. Statistical analysis was done by using SPSS, version 16.0 p-values were
calculated by chi-square test, ANOVA unpaired t-test. The p <0.05 was considered statistically significant.
Results: It was found that microalbuminuria among hypertensive patients increased steadily with the advancing age and
the duration of hypertension. The features of high urinary microalbumin 52.09±8.62 mg/24hr and the urinary creatinine
2.37±0.86mg/dl were prevalent in hypertensive patients and it increased in both male and female patients.
Conclusions: The prevalence of microalbuminuria in hypertensive individuals is high, and it revealed strong
association between microalbuminuria and hypertension. Our findings suggest that microalbuminuria could be a useful
marker to assess risk stratification and management of cardiovascular disease and renal disease.
Key words: Hypertension, Cardiovascular disease, Renal disease, Risk factors, Age factors, Urinary creatinine,
Urinary microalbumin
ASH13 Scott Hall and Robb Wolf — Evaluation of the Impact of a Paleolithic Di...Ancestral Health Society
Traditional cardiovascular risk factors including cholesterol may not provide the best tools for predicting individuals at risk for future cardiovascular disease and current insulin resistance. Novel and emerging evaluations of lipoproteins may provide a more accurate assessment of future cardiovascular risk. In an observational study of a small group of law enforcement officers, we studied the changes in both traditional and nontraditional risk factors when instructed in a “paleo” diet over 6 months. Overall, we found an encouraging impact on both traditional and nontraditional risk factors over the course of the study. It is proposed that a “paleo” diet supplemented with exercise has a positive effect on cardiovascular risk factors and may be a treatment recommendation for individuals at risk.
Blood biomarkers of smoking induced oxidative dna damage and oxidant-antioxidantUsama Mohamed El-Barrany
Abstract
Background: Smoking enhances oxidative stress by causing an imbalance between oxidants and antioxidants in the body leading to deleterious effects on various tissues. 8-hydroxy-2'-deoxyguanosine (8-OHdG) is a predominant form and a biomarker of free radical-induced oxidative lesions. This study aimed to estimate blood 8-OHdG level as a biomarker of oxidative DNA damage in active, passive as well as non-smokers and to assess its relation with lifestyle determinants as well as its effects on oxidant/antioxidant status.
Results: There were highly statistically significant higher levels of 8-OHdG, cotinine and malondialdehyde (MDA) and lower levels of superoxide dismutase (SOD) and total antioxidant capacity (TAC) in active smokers compared to both passive and non-smokers with no similar findings between the latter groups. There were no significant associations between 8-OHdG level and smoking habits, age, exercise, tea and coffee consumption as well as body mass index (BMI) among the 3 studied groups.
Conclusion: Smoking may induce oxidative stress not only through increasing the production of oxygen free radicals but also through weakening of the antioxidant defense mechanisms. Further studies are required to reach a concurrence on the background of 8-OHdG level.
Keywords: Smoking, Oxidative, Stress, Antioxidant, 8-OHdG.
Emotions are a form of non verbal communication that we use to reflect our physiological and mental state. We express emotions when we are dealing with everything around us even with our computers. Since we are becoming more dependent on computers in our lives, we need to design more interactive systems. In other words, we need to adapt computers to our needs as well as to our behavior; make computers emotionally intelligent, in order to be able to detect ours mood and make decisions based on that.
Lowering barriers to publishing biological data on the webBrad Chapman
Short 10 minute talk encouraging bioinformatics programmers to organize and reuse code targeted at making data easily available on the web. Current open source technologies are combined into a higher level framework. An example implementation using Google App Engine and existing bioinformatics libraries is presented.
A 60-minute webinar presented by Core Compliance & Legal Services and sponsored by LiveOffice.
Once You Archive Email, What's Next?
When it comes to email compliance, preparedness is key.
View this crash course in email compliance, and find out what else you need to know to protect yourself and your business.
You'll learn:
- What you are required to do after you capture electronic data
- What SEC and FINRA rules apply to email
- What types of communications require email supervision and more
Project about build a robot which is able to interact with a user in a somehow natural and intuitive way. This under the big umbrella of building embodied technologies which interact with people as a learning companion.
60-minute webinar presented by Core Compliance & Legal Services and sponsored by LiveOffice.
View this third and final crash course in email compliance, and find out how to conduct a mock audit to ensure you are prepared when the auditor knocks.
You’ll learn:
- What is required in your policies and procedures
- What you should focus on during compliance reviews
- What is required to properly store your messages and more
CANCER ETIOLOGYMutational signatures associated withtoba.docxRAHUL126667
CANCER ETIOLOGY
Mutational signatures associated with
tobacco smoking in human cancer
Ludmil B. Alexandrov,1,2,3* Young Seok Ju,4 Kerstin Haase,5 Peter Van Loo,5,6
Iñigo Martincorena,7 Serena Nik-Zainal,7,8 Yasushi Totoki,9 Akihiro Fujimoto,10,11
Hidewaki Nakagawa,10 Tatsuhiro Shibata,9,12 Peter J. Campbell,7,13 Paolo Vineis,14,15
David H. Phillips,16 Michael R. Stratton7*
Tobacco smoking increases the risk of at least 17 classes of human cancer. We analyzed
somatic mutations and DNA methylation in 5243 cancers of types for which tobacco
smoking confers an elevated risk. Smoking is associated with increased mutation burdens
of multiple distinct mutational signatures, which contribute to different extents in different
cancers. One of these signatures, mainly found in cancers derived from tissues directly
exposed to tobacco smoke, is attributable to misreplication of DNA damage caused by
tobacco carcinogens. Others likely reflect indirect activation of DNA editing by APOBEC
cytidine deaminases and of an endogenous clocklike mutational process. Smoking is
associated with limited differences in methylation. The results are consistent with
the proposition that smoking increases cancer risk by increasing the somatic mutation
load, although direct evidence for this mechanism is lacking in some smoking-related
cancer types.
T
obacco smoking has been associated with
at least 17 types of human cancer (Table 1)
and claims the lives of more than 6 million
people every year (1–4). Tobacco smoke is a
complex mixture of chemicals, among which
at least 60 are carcinogens (5). Many of these are
thought to cause cancer by inducing DNA damage
that, if misreplicated, leads to an increased bur-
den of somatic mutations and, hence, an elevated
chance of acquiring driver mutations in cancer
genes. Such damage often occurs in the form of
covalent bonding of metabolically activated re-
active species of the carcinogen to DNA bases,
termed DNA adducts (6). Tissues directly exposed
to tobacco smoke (e.g., lung), as well as some
tissues not directly exposed (e.g., bladder), show
elevated levels of DNA adducts in smokers and,
thus, evidence of exposure to carcinogenic com-
ponents of tobacco smoke (7, 8).
Each biological process causing mutations in
somatic cells leaves a mutational signature (9).
Many cancers have a somatic mutation in the
TP53 gene, and catalogs of TP53 mutations com-
piled two decades ago enabled early exploration
of these signatures (10), showing that lung can-
cers from smokers have more C>A transversions
than lung cancers from nonsmokers (11–14). To
investigate mutational signatures using the thou-
sands of mutation catalogs generated by systematic
cancer genome sequencing, we recently described
a framework in which each base substitution
signature is characterized using a 96-mutation
classification that includes the six substitution
types together with the bases immediately 5′ and
3′ to the mutated base (15). The analysis extracts
mutatio ...
The IOSR Journal of Pharmacy (IOSRPHR) is an open access online & offline peer reviewed international journal, which publishes innovative research papers, reviews, mini-reviews, short communications and notes dealing with Pharmaceutical Sciences( Pharmaceutical Technology, Pharmaceutics, Biopharmaceutics, Pharmacokinetics, Pharmaceutical/Medicinal Chemistry, Computational Chemistry and Molecular Drug Design, Pharmacognosy & Phytochemistry, Pharmacology, Pharmaceutical Analysis, Pharmacy Practice, Clinical and Hospital Pharmacy, Cell Biology, Genomics and Proteomics, Pharmacogenomics, Bioinformatics and Biotechnology of Pharmaceutical Interest........more details on Aim & Scope).
All manuscripts are subject to rapid peer review. Those of high quality (not previously published and not under consideration for publication in another journal) will be published without delay.
Es un articulo acerca de las lesiones que pueden producir el cigarrillo electrónico en cavidad oral, que consideraciones debemos tener en cuenta y como tratarlo
Abstract— Cigarette smoking is one of the major causes of cancer and cardiovascular diseases leading to millions of premature deaths each year all over the world. Scientists have identified about 4,000 different substances in tobacco all of which have certain degree of toxic effects. At least 43 of them known carcinogens.
Objective: The aim of this study is to assess the extent of adverse effect of cigarette and shisha on haematological parameters in male population of Khartoum State – Sudan.
Subject and Methods: One hundred and fifty male subjects participated in this study, cigarette smoker (n= 50), shisha smoker (n= 50) and non-smoker (n= 50). The smokers were regularly smoking at least for 10 years. Fresh peripheral blood samples from healthy adult non-smokers and smokers (males) were collected and analysed for Red Blood Cells (RBC) count, haemoglobin (Hb) content, packed cell volume (PCV), MCV, MCH and MCHC, total and differential leucocytes (WBC) counts and total platelets count by using fully automatic haematological analyser.
Results: The smokers of cigarette and shisha had significantly higher level of Hb, HCT, RBCs, TWBC count and MCHC. However, platelets counts were significantly lower in cigarette smokers than that of non-smokers. Study shows that the duration of smoking had no significant effect on haematological parameters except Hb.
Conclusion: It concluded that smoking alters haematological parameter that is injurious to health.
Effects of substituting cigarettes with e-cigarettes in adult smokers Fontem Ventures
Measurement of cardiovascular and pulmonary function endpoints
and other physiological effects following partial or complete
substitution of cigarettes with electronic cigarettes in adult smokers
An Overview on the Impact of Smoking Tobacco on Male Infertilityijtsrd
Numerous studies have revealed that sperm parameters, seminal plasma, and a number of other fertility factors are all adversely impacted by cigarette smoke. However, it is unclear how smoking actually affects male fertility. The relationship between smoking and the parameters of semen is based on the biological fact that smoking increases the presence of reactive oxygen species, leading to oxidative stress OS . Male fertility is decreased as a result of OSs devastating effects on sperm parameters like viability and morphology as well as its impairment of sperm function. Not all studies, though, have reached the same conclusions. The debated relationship between smoking and male fertility is clarified by this review, which also examines the effect of different smoking methods on male infertility. Additionally, this review highlights the mechanism how tobacco smoking disrupts the entire male reproductive system. Monika Singh "An Overview on the Impact of Smoking Tobacco on Male Infertility" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-7 | Issue-1 , February 2023, URL: https://www.ijtsrd.com/papers/ijtsrd52773.pdf Paper URL: https://www.ijtsrd.com/biological-science/other/52773/an-overview-on-the-impact-of-smoking-tobacco-on-male-infertility/monika-singh
12 weeks Switch to Vaping: Science of Vaping Fontem Ventures
A randomised, parallel group clinical study was performed to evaluate the safety profile of an e-vapour
product (EVP; 2.0% nicotine) in smokers of conventional cigarettes (CCs) switching to use the EVP for 12
weeks.
Genotoxic and Reprotoxic Effects of Afabazole Tobacco Smokeijtsrd
The harms of smoking are well known. Smokers are more likely to develop lung cancer and other malignant tumors, cardiovascular pathologies and chronic respiratory diseases. The genotoxic and reprotoxic effects of Afabazole tobacco smoke are discussed in detail in this article. Ergashkulov Mexroj Xurshedovich | Yuldashev S. J. "Genotoxic and Reprotoxic Effects of Afabazole Tobacco Smoke" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-6 | Issue-4 , June 2022, URL: https://www.ijtsrd.com/papers/ijtsrd50040.pdf Paper URL: https://www.ijtsrd.com/medicine/ophthalmology/50040/genotoxic-and-reprotoxic-effects-of-afabazole-tobacco-smoke/ergashkulov-mexroj-xurshedovich
In this study the effect of cigarette smoking on
semen quality of fertile and infertile men with or without obesity
was investigated.
The number of fertile and infertile participants was as
following: 203 fertile smokers, 78 fertile non-smokers, 147
infertile smokers and 68 infertile non-smokers. The body mass
index (BMI) was measured in all fertile and infertile men. All
semen parameters were assessed in both fertile and infertile men
with or without obesity to identify the values that would
distinguish fertile from infertile men.
The results of this study showed that cigarette smoking has a
significant influence only on sperm count, percentage of active
sperm and sperm morphology. The semen parameters in infertile
men were significantly different from that of fertile men. The
influence of body mass index on semen parameters was obvious
except in percentage of immotile sperms. This results suggest
that the chemical agents or mutagens may affect male
reproductive via direct effect on the spermatogenesis
Articles/Carcinogen+Exposure.pdf
Carcinogen Exposure during Short-term Switching
from Regular to ‘‘Light’’ Cigarettes
Neal L. Benowitz,1 Peyton Jacob III,1 John T. Bernert,2 Margaret Wilson,1 Langing Wang,2
Faith Allen,1 and Delia Dempsey1
1Division of Clinical Pharmacology and Experimental Therapeutics, Departments of Medicine, Psychiatry, and Biopharmaceutical Sciences,
University of California, San Francisco and 2Biomarkers Laboratory, Emergency Response and Air Toxicants Branch, Division of Laboratory
Science, National Center for Environmental Health, Centers for Disease Control, Atlanta, Georgia
Abstract
Objectives: ‘‘Light’’ cigarettes are extremely popular and
are perceived by many smokers as less hazardous than
higher-yield cigarettes. The objectives of this study were
(a) to assess a battery of biomarkers of tobacco smoke
exposure that includes tobacco smoke carcinogens, (b) to
examine the behavioral nature of compensation, and (c) to
examine the consistency of an individual’s tobacco smoke
exposure when smoking the same cigarette at different
times.
Methods: The study was a 3-week crossover study in which
smokers smoked their usual cigarettes during weeks 1 and 3,
and a light cigarette, with a machine-determined nicotine
yield of about 50% of the usual cigarette, during week 2.
Blood and urine biomarkers of exposure and subjective
questionnaires were collected weekly.
Results: Based on cotinine and carboxyhemoglobin levels,
compensation averaged 78% and 83%, respectively. Urinary
excretion of 4-(methylnitrosamino)-1-(3-pyridyl)-butanol, a
metabolite of the tobacco specific carcinogen 4-(methylnitro-
samino)-1-(3-pyridyl)-butanone, and a number of polycyclic
aromatic hydrocarbon metabolites was similar in all con-
ditions. Compensation was accomplished both by smoking
cigarettes more intensively and by smoking more cigarettes
per day. Exposures to various tobacco smoke constituents
while smoking the usual brand of cigarette in weeks 1 and 3
were highly correlated.
Conclusion: Our findings support the idea that smokers
compensate to a high degree when switched from their usual
brand to a light cigarette. Short-term switching resulted in no
significant reduction in carcinogen exposure. Our assess-
ment, based on measures of biochemical exposures, supports
the idea that switching to light cigarettes is unlikely to
reduce the health risks of cigarette smoking. (Cancer
Epidemiol Biomarkers Prev 2005;14(6):1376 – 83)
Introduction
Cigarette smoking is sustained by addiction to nicotine (1).
Dependent smokers tend to regulate their intake of nicotine
from day to day. When switched to cigarettes of lower
machine-determined yield, smokers on average increase their
intake of nicotine beyond that which would be expected based
on the stated (machine tested) yield (2, 3). The process of
smoking lower-yield cigarettes more intensively than higher-
yield cigarettes is termed compensation. When compensating
for lower nicotine yields, smoker ...
15. To investigate the association between
smoking and the risk of VTE among
middle-aged men and women.
Severinsen MT, Department of Clinical Epidemiology, Aarhus University
Hospital, Aalborg, Denmark. J Thromb Haemost. 2009 Aug;7(8):1297-303
OBJECTIVE
16. ◦ Danish prospective study 'Diet, Cancer and Health'.
◦ 1993 to 1997
◦ 27,178 men and 29,875 women,
◦ 50-64 years
17. ◦ 641 incident cases of VTE were verified.
◦ Positive association between current smoking and VTE,
OR 1.52 (1.15-2.00) for smoking women
OR 1.32 (1.00-1.74) for smoking men
Positive dose-response relationship.
◦ Former smokers had the same hazard as never
smokers.
J Thromb Haemost. 2009 Aug;7(8):1297-303
RESULTS
18. - Smoking was an independent risk factor for VTE
- Former smokers have the same risk of VTE as never
smokers, indicating the potential benefits of smoking
cessation.
J Thromb Haemost. 2009 Aug;7(8):1297-303
19. To conduct a prospective, population-based cohort
study to investigate the association between cigarette
smoking and the risk of incident VTE.
OBJECTIVES :
J Thromb Haemost. 2012 Oct;10(10):2068-74
20. – Information on smoking habits was assessed by self-
administered questionnaires in 24 576 subjects
– 25-96 years
– 1994-1995
– Incident cases of VTE were registered until the end of
follow-up at 1 September 2007 (median of 12.5 y)
PATIENTS/METHODS:
J Thromb Haemost. 2012 Oct;10(10):2068-74
21. ◦ 389 incident VTE events (1.61 per 1000 pers-y)
◦ Heavy smokers (> 20 pack-years) compared with
never smokers.
HR : 1.46 (1.04-2.05) for total VTE,
HR :1.75 (1.14-2.69) for provoked VTE
RESULTS :
J Thromb Haemost. 2012 Oct;10(10):2068-74
22. ◦ The risk of provoked VTE increased with more
pack-years of smoking (P = 0.02).
◦ Smoking was not associated with risk of
unprovoked VTE.
◦ Association between pack-years of smoking and
VTE disappeared when occurrence of cancer or
myocardial infarction.
RESULTS :
J Thromb Haemost. 2012 Oct;10(10):2068-74
23. BACKGROUND
The evidence for an association between smoking
and venous thrombosis (VT) is inconsistent, and
its mediation pathways remain to be fully
elucidated.
Thromb Haemost. 2013 Mar 7;109(5)
24. A population-based, case-control study was
conducted in healthcare system in Washington State.
Cases were women aged 18-90 years who
experienced a validated incident deep vein
thrombosis or pulmonary embolism between
January 1, 1995, and December 31, 2009.
METHODS :
Thromb Haemost. 2013 Mar 7;109(5)
25. ◦ Controls were randomly selected from members of the
healthcare system.
◦ Smoking status (current, former, never) was assessed from
medical records review and, for a subset, also by telephone
interview.
◦ Multivariable logistic regression was used to estimate odds
ratios (OR) associated with smoking status.
METHODS :
Thromb Haemost. 2013 Mar 7;109(5)
26. RESULTS :
◦ We identified 2,278 cases and 5,927 controls.
◦ Subjects comprised mostly postmenopausal white
women with a mean age of 66 years and a
current smoking prevalence of 10%.
◦ Compared to never-smokers, current and former
smokers were at higher risk of VT (adjusted OR
1.21, [CI] 1.02-1.44 and OR 1.15, CI 1.03-1.29.
◦ These associations were attenuated for
potential mediators (cardiovascular
disease, congestive heart failure, cancer, recent
hospitalisations and physical activity): OR 1.02 CI
(0.83-1.25) and 0.95 CI (0.83-1.08).
Thromb Haemost. 2013 Mar 7;109(5)
27. The modestly increased risk of VT in women who
are current or former smokers might be explained
by the occurrence of smoking-related diseases
and decreased physical activity.
Our results do not support a direct biological effect
of smoking on the risk of VT that is clinically
relevant
Thromb Haemost. 2013 Mar 7;109(5)
28. La relation existe entre les fumeurs et la
thrombose veineuse
Mais elle est atténuée quand elle est ajustée avec
des maladies potentielles (Maladie cardio-
vasculaire, cancer…)
Relation indirecte
29.
30.
31. carbon monoxide, a product of cigarette smoking, has
been demonstrated to enhance plasmatic
coagulation in vitro via modulation of a heme
associated with fibrinogen.
We hypothesized that plasmatic hypercoagulability
and formation of carboxyhemefibrinogen (COHF)
detected would be observed after cigarette smoking
Blood Coagul Fibrinolysis. 2013 Feb 21
32. Smoking participants (n : 20) two cigarettes
consumed within 90 min : plasma collected and
normal participant (n = 20) plasma was also
obtained.
Thrombelastographic analyses revealed that
plasma obtained from smokers had an 86%
greater velocity of clot growth and 65% larger clot
strength than normal participant plasma.
Blood Coagul Fibrinolysis. 2013 Feb 21
33. We conclude that smoking induced a
hypercoagulable state and COHF formation in
an important portion of participants tested.
Future investigations of the effects
of smoking, plasmatic hypercoagulation and
COHF formation are planned in populations
with established atherosclerotic/ thrombotic
disease
Blood Coagul Fibrinolysis. 2013 Feb 21
34. 2) Exposure to acrolein by inhalation causes platelet
activation
35. The purpose was to determine whether CO and NO
diminished fibrinolysis by enhancement of α₂-
antiaplasmin via a putative heme group.
Blood Coagul Fibrinolysis. 2011 Dec;22(8):712-
9
36. CO significantly enhanced α₂-antiplasmin activity, but
decreased plasmin activity.
NO decreased both α₂-antiplasmin and plasmin activity.
Diminished fibrinolysis
Blood Coagul Fibrinolysis. 2011 Dec;22(8):712-9
37. Objective :
◦ Smokers exhibit higher circulating levels of tissue factor (TF)
than do non smokers, but the underlying mechanisms have not
been reported.
◦ we investigated whether exposure of human
monocyte/macrophages to tobacco smoke induces their release
of MVs and whether these MVs are procoagulant.
Arterioscler Thromb Vasc Biol. 2010 September ; 30(9): 1818–1824.
4) Tobacco Smoke Induces the generation of Progoagulant
Microvesicles from Human Monocyte/Macrophages
38. RESULTS :
◦ Exposure of human monocytes and
macrophages to tobacco smoke extract
significantly increased their total and TF-
positive MV generation.
4) Tobacco Smoke Induces the generation of Progoagulant
Microvesicles from Human Monocyte/Macrophages
Arterioscler Thromb Vasc Biol. 2010 September ; 30(9): 1818–1824.
39. Monoxide de carbone: entraine un état
d’hypercoagulable et la formation de COHF
Acroleine : active les plaquettes
Monoxide de carbone et Nitric oxide diminuent la
fibrinolyse
L’exposition des monocytes et des
macrophages humaines au tabac augmente
signifiquement le facteur Tissulaire et la
génération des MV.
40.
41. • Retrospective observational study among 350 patients
receiving a stable dose of warfarin for at least 2 weeks. The
primary objective of the study was to assess the
relationship between clinical factors, including smoking with
non therapeutic INR results. Based on a univariate
analysis, smoking was not significantly associated with
non therapeutic INR.
. McGriff-Lee NJ et al. Ann Pharmacother 2005 3912 1996-2002
42. Prospective observational study among 80
patients with heart failure receiving warfarin
therapy to assess the relationship among various
clinical factors, including smoking with non
therapeutic INR (defined as having > 25% of INR
out of range throughout the study period). Using
the Pearson correlation method, the authors
found no significant relationship of smoking
and non therapeutic INR
Pamboukian SV et al. Clin Cardiol 2008 311 30-34
43. BACKGROUND:
Chronic smoking, theoretically, can interfere with
warfarin metabolism through enzyme-inducing
effects of polycyclic aromatic hydrocarbons.
However, clinical evidence of interactions between
warfarin and smoking are inconclusive.
This study aimed to systematically review all
relevant clinical evidence of this interaction.
CHEST. 2011;139(5):1130-1139
44. METHODS:
We performed a systematic search using
computerized databases, from 1966 to December
2008.
Keywords included "warfarin" with "smoking,"
"tobacco," "cigarette," and "polycyclic aromatic
hydrocarbons."
All articles were reviewed independently by two
investigators for study
design, population, outcomes, and quality of
evidence.
45. RESULTS:
Of the 1,240 studies retrieved one experimental:
pharmacokinetic study and 12 cross-sectional
studies.
“smoking was associated with a 12.13% (95%
CI, 6.999-17.265; P < .001) increase in warfarin
dosage requirement and an additional 2.26 mg
(95% CI, 2.529-7.042; P = .355) per week
compared with nonsmoking”.
48. Conclusion :
Evidence suggests that smoking may
potentially cause significant interaction with
warfarin by increasing warfarin
clearance, which leads to reduced warfarin
effects.
49. Effet du tabac sur l’INR : les anciennes études ne
montraient pas de relation
Tabagisme et warfarine : relation évidente par
augmentation de la clearance et réduction de son
l’effet